Intrauterine growth restriction impacts tolerance to total parenteral nutrition in extremely low birth weight infants

被引:32
作者
Baserga M.C. [1 ]
Sola A. [2 ]
机构
[1] Department of Pediatrics, Children's Hospital of Orange County, Orange, CA
[2] Division of Neonatology, Department of Pediatrics, Emory University, Atlanta, GA 30322
关键词
D O I
10.1038/sj.jp.7211137
中图分类号
学科分类号
摘要
Background: Hepatobiliary dysfunction is well recognized as a complication of long-term total parenteral nutrition (TPN). Because intrauterine growth restriction (IUGR) alters a number of metabolic and physiologic variables in the fetus that probably affect the hepatocyte function and tolerance to feedings in the IUGR extremely low birth weight (ELBW), we hypothesized that this group of babies would have an increased incidence of TPN-associated cholestasis and chronic liver failure. Methods: We performed a review of all ELBW infants (birth weight < 1000 g) that received TPN for >7 days. Results: Among 1768 infants admitted to the neonatal intensive care unit there were 103 ELBW who received TPN > 7 days, 38 (37%) of them developed TPN cholestasis. Among 69 appropriate for gestational age (AGA)-ELBW infants, 19 (27%) developed cholestasis compared to 19/34 small for gestational age (SGA)-ELBW infants (56%) (p<0.0009). Maximum direct bilirubin values and days on TPN were similar in both groups. SGA-ELBW infants had an increased incidence and earlier onset of cholestasis when compared to AGA-ELBW patients. Liver biopsies and/or autopsies of infants that developed liver failure (four AGA/four SGA) showed extensive sinusoidal/portal fibrosis compatible with "TPN lesion". In the other 30 cases, liver function eventually returned to normal after TPN discontinuation. Conclusions: When compared, SGA-ELBW infants who received TPN >7 days, despite being more mature than AGA-ELBW infants, have an increased risk for TPN cholestasis and developed this complication earlier in life. However, the incidence of chronic liver failure was not different in these two groups. © 2004 Nature Publishing Group. All rights reserved.
引用
收藏
页码:476 / 481
页数:5
相关论文
共 19 条
[11]  
Boehm G., Muller D.M., Teichmann B., Krumbiegel P., Influence of intrauterine growth retardation on parameters of liver function in low birth weight infants, Eur. J. Pediatr., 149, pp. 396-398, (1990)
[12]  
Boehm G., Senger H., Muller D., Beyreiss K., Raiha N.C., Metabolic differences between AGA- and SGA-infants of very low birthweight. II. Relationship to protein intake, Acta. Pediatr. Scand., 77, pp. 642-646, (1988)
[13]  
Boehm G., Senger H., Braun W., Beyreiss K., Raiha N.C., Metabolic differences between AGA- and SGA-infants of very low birthweight. I. Relationship to intrauterine growth retardation, Acta. Paediatr. Scand., 77, pp. 19-23, (1988)
[14]  
Lane R., Flozack A., Ogata E., Bell G.I., Simmons R., Altered hepatic gene expression of enzymes involved in energy metabolism in the growth-retarded fetal rat, Pediatr. Res., 39, pp. 390-394, (1996)
[15]  
Lane R.H., Kelley D.E., Gruetzmacher E.M., Devaskar S.U., Uteroplacental insufficiency alters hepatic fatty acid-metabolizing enzymes in juvenile and adult rats, Am. J. Physiol. Regul. Integr. Comp. Physiol., 280, (2001)
[16]  
Barker D.J., Fetal origins of coronary heart disease, BMJ, 311, 6998, pp. 171-174, (1995)
[17]  
Li S., Nussbaum M.S., Teague D., Gapen C.L., Dayal R., Fischer J.E., Increasing dextrose concentrations in total parenteral nutrition (TPN) causes alterations in hepatic morphology and plasma levels of insulin and glucagon in rats, J. Surg. Res., 44, pp. 639-648, (1988)
[18]  
Lane R.H., Crawford S.E., Flozak A.S., Simmons R.A., Localization and quantification of glucose transporters in liver of growth-retarded fetal and neonatal rats, Am. J. Physiol., 276, 1 PART 1, (1999)
[19]  
Lee M.J., Conner E.L., Charafeddine L., Woods Jr. J.R., del Priore G., A critical birth weight and other determinants of survival for infants with severe intrauterine growth restriction, Ann. NY Acad. Sci., 943, pp. 326-339, (2001)